Hydrocephalus is a disease in which the body is unable to remove cerebrospinal fluid (CSF) from the ventricles of the brain, usually due to the blockage of natural drainage paths. As a result, CSF accumulates within the skull and causes increased intracranial pressure. This increased pressure, in turn, causes adverse physiological effects including compression of brain tissue, impairment of blood flow, and impairment of normal brain metabolism.
Hydrocephalus is usually treated by installing a shunt system for draining excess CSF in a controlled manner from the production site, the cerebral ventricles, to a resorption site elsewhere in the body, such as the peritoneal cavity or the right atrium. The shunt system typically includes a proximal catheter inserted into the ventricle which is connected distally to a catheter that conducts fluid to the resorption site. To control the flow of CSF and maintain the proper pressure in the ventricles, a valve is placed in the conduit between the brain and the resorption site.
Many shunt systems simply utilize the differential fluid pressure between the production site and the resorption site to control fluid flow. However, when a patient rises from a supine position to a seated or standing position, the differential fluid pressure between the production and resorption sites normally increases due to the elevation of the brain compared with the selected drainage location elsewhere in the body. This increase in the pressure differential due to hydrostatic factors can result in overdrainage, or siphoning, of CSF from the cerebral ventricles. Failure to recreate physiological CSF outflow may result in significant stress in the cerebral tissues which in the long term can lead to effects like slit ventricle syndrome, changes in the brain compliance from glial cell hypertrophy, chronic headaches, and subdural hematomas.
More recently, antisiphon shunt systems have been developed which minimize overdrainage in upright posture to maintain pressures within limits which would normally be provided by physiological mechanisms regardless of orientation. In contrast to standard differential pressure valves, antisiphon valves close whenever the cerebral ventricular pressure becomes subatmospheric, thus eliminating siphoning effects when a patient stands. Whenever the ventricular pressure rises above atmospheric pressure, the valve opens, thus regulating ventricular pressure within a more normal range. Consequently, flow is controlled predominantly by the differential between the proximal, ventricular pressure and atmospheric pressure, rather than by the differential pressure between the production and resorption sites.
As described above, proper functioning of an antisiphon device requires exposure of the valve to atmospheric pressure. As a result, the valves are typically enclosed in chambers having walls which are deformable or are provided with apertures therein, thereby rendering the valves susceptible to changes in external, subcutaneous pressure. By construction, an increase in subcutaneous pressure above atmospheric pressure will increase the pressure within the chamber and, consequently, increase the resistance to flow. Subcutaneous fibrotic scarring which inevitably develops around the site of shunt implantation can cause significant increases in external pressure, resulting in underdrainage of CSF through the antisiphon shunt system.